Red cells of patients with sickle cell anemia were demonstrated by electron microscopy to develop polymers at venous oxygen tensions. Polymers developed in the denser cells within the time of the normal venous circulation and persisted in these cells after reoxygenation for times equivalent to the arterial circulation. The persistence of polymers was associated with a delay in the oxygen uptake that was particularly striking in the denser cells. We attribute the delay to the hemoglobin molecules of the polymers being locked in a low affinity conformation. The studies have pointed out that a portion of the red cells may develop rheologic abnormalities under conditions of the normal circulation. The delay in uptake of oxygen by sickle cells may account, in part, for the arterial hypoxemia of patients with sickle cell anemia. Fetal hemoglobin has been shown to be unstable in isopropanol -- a standard test for the detection of unstable hemoglobins. We have attributed this instability to a rapid oxidation of fetal hemoglobin. The test should be interpreted cautiously when fetal hemoglobin is present. A new, benign hemoglobin variant was described: Hb Sequoia (B 120 lys yields asn). BIBLIOGRAPHIC REFERENCES: Hahn, J.A., Messer, M.J. and Bradley, T.B. Ultrastructure of sickling and unsickling in time-lapse studies. Brit. J. Haem. 34:561, 1976. Budge, L.J., Bradley, T.B., Graham, J.L. Hemoglobin Rivadh in a Mexican American family of Spanish ancestry. Hemoglobin, 1(3): pp. 283-287, 1977.